Fig. 9.
Fig. 9. Detection of TGF-α mRNA in bone marrow and peripheral blood monocytes by in situ hybridization. (A) Bright-field photomicrograph of a section of bone marrow from a patient with myelodysplastic syndrome hybridized with 32S-labeled antisense RNA for TGF-α and stained with hematoxylin and eosin. Positive signal for TGF-α is seen in numerous monocytoid cells (closed arrows), but not in the red blood cells (open arrows). Autoradiography was for 30 days. (×1,000). (B) Wright-Giemsa stained section of a surrounding region of the bone marrow. Monocytoid cells (arrows) are abundant in this area (×100). (C) and (D) Dark-field photomicrographs of circulating monocytes, prepared as described in Materials and Methods. There is no autoradiographic signal for TGF-α mRNA (C), whereas specific signal appearing as bright dots under dark-field microscopy, was evident for β-actin mRNA (D). Autoradiography was for 32 days. (×256).

Detection of TGF-α mRNA in bone marrow and peripheral blood monocytes by in situ hybridization. (A) Bright-field photomicrograph of a section of bone marrow from a patient with myelodysplastic syndrome hybridized with 32S-labeled antisense RNA for TGF-α and stained with hematoxylin and eosin. Positive signal for TGF-α is seen in numerous monocytoid cells (closed arrows), but not in the red blood cells (open arrows). Autoradiography was for 30 days. (×1,000). (B) Wright-Giemsa stained section of a surrounding region of the bone marrow. Monocytoid cells (arrows) are abundant in this area (×100). (C) and (D) Dark-field photomicrographs of circulating monocytes, prepared as described in Materials and Methods. There is no autoradiographic signal for TGF-α mRNA (C), whereas specific signal appearing as bright dots under dark-field microscopy, was evident for β-actin mRNA (D). Autoradiography was for 32 days. (×256).

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